A goal of cardiac pacing therapy is to “capture” heart tissue, typically through administration of an electrical stimulus, e.g., a pacing pulse. Capture is achieved when an applied stimulus causes depolarization (contraction) of the heart's myocardial tissue. The stimulation-capture process allows for therapeutic management of various cardiac functions. For example, abnormal heart tissue contractions, known as arrhythmias, which include bradycardia (slow heart rate), tachycardia (fast heart rate), any markedly irregular rhythm, blocks and/or the presence of premature contractions, are manageable through use of stimulation-capture therapies.
Arrhythmias are often problematic and interfere with a heart's normal pumping function. In a normal heart, a pump cycle beings with a natural (or intrinsic) stimulus originating at the sinoatrial node, which then travels to intranodal atrial conduction tracts and the Bachmann's bundle and causes the atria to contract and pump blood into the ventricles. The stimulus next travels to the atrioventricular node, the Bundle of His, and the Purkinje system where the stimulus causes simultaneous contraction of the right ventricle, which pumps deoxygenated blood to the lungs through the pulmonary artery, and the left ventricle, which pumps oxygenated blood to the body through the aorta, the body's main artery. In an arrhythmic heart, the stimulation process is corrupt and capable of disabling the heart's pumping action. Pacing therapy seeks to terminate or overcome arrhythmic processes and allow the heart to function normally.
One method of terminating an arrhythmic process involves delivering a single cardioversion level electrical stimulus to the heart. After the stimulus, if the heart does not return to a satisfactory intrinsic rate, or an intrinsic beat is not established, then pacing therapy may continue on a beat-by-beat basis. In most beat-by-beat therapies, an implantable device monitors the heart and then determines whether a pacing stimulus is needed. In such therapies, a situation calling for a stimulus is the absence of intrinsic stimulation. An effective beat-by-beat pacing device therefore includes features to determine the need for a stimulus, to deliver a stimulus in a timely manner, and to ensure that a stimulus does not greatly exceed the energy level required to capture the heart. Most implantable stimulation devices operate on a limited power supply; thus, the features to determine the need for a stimulus and to control the power thereof act to prolong the life of the device. The determination and timely delivery features are useful in avoiding a condition known as fusion.
Fusion is commonly defined as cardiac depolarization that occurs in response to both an intrinsic stimulus and an applied electrical stimulus with cardiac depolarization (atrial or ventricular) resulting from more than one focus, e.g., two foci, one corresponding to the intrinsic stimulus and one corresponding to the applied stimulus. Evidence of fusion appears in polarization changes of active cardiac tissue, which can be sensed through electrodes placed on or within the heart. The measured or recorded signal from such electrodes is generally referred to as an intracardiac electrogram (IEGM). An IEGM provides valuable information as to the functioning of a patient's heart. For example, recordation of intrinsic ventricular depolarization results in a prominent IEGM waveform, classified as the QRS complex or R-wave. R-wave characteristics, as seen in an IEGM, reflect the presence of polarization changes resulting from both intrinsic and non-intrinsic activity. Because fusion is a combination of intrinsic and non-intrinsic activity, fusion often results in a distorted IEGM R-wave (QRS complex).
Fusion includes the terms “fusion beat”, wherein an applied stimulus is delivered just prior to the arrival at the electrodes of an intrinsically generated and propagating R-wave, which affects the ventricular depolarization.
U.S. Pat. No. 5,836,984, entitled “Heart stimulating device”, to Obel, assigned to Pacesetter AB, issued Nov. 17, 1998 ('984 patent), discusses pacemakers of the inhibition type wherein IEGM signals are sensed via a lead and electrode arrangement. Intrinsic and stimulated QRS waves in the IEGM signals are monitored by sensing circuitry in the pacemaker. According to the '984 patent, as long as intrinsic QRS complexes are detected at an acceptable rate by the sensing circuitry, the pacemaker inhibits stimulation. At each detected intrinsic QRS complex, a timer is started in the pacemaker. If no new QRS complex is detected within a predetermined basic interval of the timer, a stimulation pulse to the heart is emitted by a pulse generator in the pacemaker.
A problem noted by the '984 patent involves QRS complex detections that are performed after a bandpass filter, which delays the IEGM signals. In this situation, if an intrinsic QRS complex occurs immediately before the end of a basic escape interval (period between a sensed cardiac event and the next stimulation pulse), it will not be noticed before the next stimulation pulse is delivered. Consequently, when the next stimulation pulse is delivered, the pacemaker will have difficulties in detecting the QRS complex and, as a result of the non-detection, the pacemaker may react by increasing its output energy, even though such an increase is not needed. The '984 patent suggests that problems become more severe if the intrinsic heart rhythm is somewhat faster than that of the pacemaker and that a continuous state of this type could be avoided by using so-called hysteresis.
Hysteresis is a programmable feature available in some pacemakers that allows programming of a hysteresis escape rate (associated with the escape interval) that is lower than the programmed base rate (rate of stimulation pulses in the absence of intrinsic activity). Hysteresis may be accomplished by prolonging the pacing interval (time period between consecutive stimulation pulses without an intervening sensed event) following a sensed intrinsic beat.
The problem discussed in the '984 patent can lead to a higher energy consumption rate than necessary because the heart stimulating device emits pulses that are not required. Also, the energy of the stimulation pulses may erroneously be set higher than necessary. An excessively high energy consumption will cause premature depletion of the battery of the stimulation device resulting in higher risk and inconvenience to the patient. Thus, a need exists for stimulation devices that are capable of distinguishing between a true capture failure and a fusion beat.
Accordingly, there is a need for pacing therapies that better classify capture and fusion events.